Ultraviolet-irradiated apoptotic lymphocytes produce interleukin-10 by themselves.

Since inflammatory responses are rarely associated with apoptotic cell death, it is plausible that cells undergoing apoptosis may signal the immune system to suppress inflammatory responses. By employing intracytoplasmic cytokine staining in conjunction with annexin V-binding, we examined the representative pro-inflammatory cytokine tumor necrosis factor-alpha (TNFalpha) and anti-inflammatory cytokine interleukin-10 (IL-10) expression in ultraviolet (UV)-irradiated lymphocytes and analyzed them with apoptosis induction at a single cell level. We show here that lymphocytes exposed to UV resulted in IL-10 expression with marginal TNFalpha expression, and these IL-10-expressing cells underwent apoptosis. Addition of inhibitors for caspases blocked UV-induced apoptosis but not IL-10. These results indicate that UV elicited at least two types of signals: one which was caspase dependent, leading to apoptosis; and another which was caspase independent, leading to IL-10 production. Lymphocyte apoptosis was thus found to link anti-inflammatory cytokine secretion, and thereby may contribute to preventing unwanted immune responses.